Parathyroid hormone and hypertension.

Numerous studies in humans and experimental models have shown that alterations in calcium homeostasis are associated with an increased risk of cardiovascular complication. In particular, changes in systemic calcium metabolism are thought to play an important role in the regulation of blood pressure. One hypothesis for this link implicates parathyroid hormone (PTH). Serum calcium level is tightly regulated by PTH in a classic negativefeedback system. A small decrease in serum calcium stimulates an abrupt increase in PTH secretion, which leads to calcium mobilization from bone, increased renal tubular calcium reabsorption and increased renal hydroxylation of 25-hydroxyvitamin D to the biologically more active 1,25-dihydroxyvitamin D (which enhances calcium absorption from the intestine). Factors that tend to reduce the serum calcium levels (i.e. vitamin D deficiency) induce secondary hyperparathyroidism. In primary hyperparathyroidism, there is an autonomous increase in PTH secretion resulting in hypercalcaemia. Several studies have reported a positive correlation between serum PTH levels and hypertension [1]. This relationship has been demonstrated in patients with primary hyperparathyroidism as well as in those with secondary hyperparathyroidism [1]. Moreover, some studies have shown that patients with essential hypertension have a higher serum concentration of PTH than normotensive individuals. These data have led to the speculation that PTH may be involved in the pathogenesis of hypertension.